Cocaine transiently impairs maternal behavior in the rat.

This paradigm distinguished between two hypotheses not previously directly addressed. Do repeated exposures to cocaine at critical times during pregnancy, when the neural mechanisms that support maternal behavior are being readied, alter some fundamental neural underpinning of maternal behavior in rats? Alternatively, does cocaine alter maternal behavior only when circulating? During the 4 hr after cocaine injection (20 or 40 mg/kg), there were significant deficits in maternal behavior. In contrast, 16 hr after cocaine injection, drug-injected females, in which plasma cocaine had fallen to nondetectable levels, showed the normal maternal behavior of saline-injected controls. This pattern of impaired maternal behavior after cocaine injection, followed by normal behavior as blood levels returned to zero, was replicated over 8 days. It was concluded that cocaine impairs maternal behavior only when circulating and does not have a residual effect in the transiently drug-free, chronically drug-treated dam. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Plasma cocaine levels and locomotor activity after systemic injection in virgin and in lactating maternal female rats

We have determined the temporal pattern of plasma cocaine levels and increased activity that result from acute systemic injections of cocaine to female rats in two different endocrine and behavioral states, in nonmaternal virgins and in lactating maternal dams. Plasma levels of cocaine as well as ambulatory and rearing activity were determined every 30 min for a total of 300 min after subcutaneous injections of either 10, 20, or 40 mg/kg of cocaine. Virgin females had no prior drug history, whereas lactating, maternal dams had received two cocaine injections before activity testing. Within 30 min after an injection, cocaine in the plasma and activity were substantially elevated, and generally remained so for 270-300 min. Overall, plasma cocaine levels and activity were well correlated and followed a predictable dose-response pattern. The onset, peak, duration, and decline of activity corresponded generally to the onset, peak, duration, and decline of plasma cocaine. For virgins, mean ambulatory activity increased 2.5-4.0-fold over baseline, whereas in lactating females activity increased 5-11-fold over baseline. Stereotypy did not occur. Although the general responsivity of these females to cocaine was very similar to that reported for males, there are differences in the timing of peak activity and the return of activity to baseline when the virgins and the lactating dams are compared to each other and to reports by others on male rats. These data support the hypothesis that endocrine or behavioral state may influence the responsiveness of animals to cocaine.     

Microinfusion of cocaine into the medial preoptic area or nucleus accumbens transiently impairs maternal behavior in the rat.

Cocaine was microinfused bilaterally (50 μg/0.5 μl/side) into the medial preoptic area (MPOA) or nucleus accumbens (NA), 2 regions within the rat brain neural circuit known to mediate maternal behavior (MB). Additionally, 2 sites not involved in this neural circuit, the dorsal striatum and dorsal medial hippocampus, were used as control sites. Microinfusion of cocaine into the MPOA or NA impaired MB, whereas infusion into the control sites did not. MB impairment was not temporally coincident with the increased locomotor activity, also documented after cocaine infusion into the MPOA or NA, arguing strongly that impaired MB is a direct, specific effect of cocaine in these areas, not a derivative of increased motor activity. This is the first demonstration that cocaine action on single central nervous system (CNS) sites can impair MB to the same extent as systemic injections. Thus, cocaine's simultaneous effect on multiple CNS sites is not required for MB impairment. (PsycINFO Database Record (c) 2010 APA, all rights reserved)